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Feminisation of fish 9. Effects of (xeno-)estrogens on the reproductive success/fertility of female fish.Most studies conducted both in the field and in the laboratory have focused on the feminising potential of estrogens and xenoestrogens on the male reproductive system and the consequences for the male fertility since the most detrimental effects are suspected to be seen in the male gender due to its low endogenous levels of estrogens. During the last few years some attention has, however, also been given to the effects of the compounds on the female fertility which have demonstrated that relatively low concentration of both steroid estrogens and xenoestrogens also are capable of reducing the reproductive success of female fish. In female roach from the English rivers, in which high frequencies of intersex have been found among males, atretic and vacuolated oocytes were found. In female zebrafish a dose-related reduction in the number of spawning females were observed at three weeks exposure to 10 ng EE2/l with complete inhibition of spawning at levels of 25 ng/l (61). The non-spawning females had significantly smaller ovaries lacking mature oocytes, indicating that EE2 interfered with oocyte maturation. Another study with zebrafish resulted in reduced egg production in females exposed to 10 and 25 ng/l EE2 when exposing for a period of 4 month from the embryo stage (68). In fathead minnow exposure to 10 ng/l EE2 has also caused a reduction in the number of oviposited eggs after a 4-week exposure period (202). In a partial life-cycle test of the marine species, sheepshead minnow, a LOEC for reduction in the egg production was observed by 20 ng EE2/l in one spawning trail and by 200 ng/l in a second (31). Hatching success was also reduced among the progeny of fish exposed to 200 ng/l. Both males and females were exposed in this study and it was therefore possible that the reduced reproductive success was a consequence of both atresia of oocytes in the ovaries and extensive fibrosis of the testes observed at this concentration. Exposure studies on female with E2 have found reduced egg spawning in medaka at 27.2 ng/l (63) and an EC50 for inhibition of egg production in fathead minnow at 120 ng E2/l (203). Nonylphenol exposure has also reduced the egg production of females. This was seen in medaka after exposure for two weeks to 6.6 m g NP/l. In rainbow trout exposure of female fish for 18 months during early ovarian development to 85.6 m g NP/l shut off the reproduction of the female totally, since vitellogenin, although produced in large quantities, was not taken up by the oocytes (69). The oocytes therefore did not develop further. A possible explanation for this might have been the concomitantly observed suppression of follicle stimulating hormone (FSH) synthesis in the pituitary and reduced FSH level in the plasma. This gonadotophin is thought to induce the recruitment of oocytes into maturation and stimulates the uptake of vitellogenin into the developing oocytes. Reduced FSH levels in plasma were suppressed with lower concentration of NP (0.7 and 8.3 m g/l) but changes in the ovarian development was not observed at these concentrations. A study with estradiol has also demonstrated that vitellogenin can autoregulate its own synthesis by the liver in females via down-regulation of the E2-production of the oocytes (204). Vitellogenin synthesis is as earlierdescribed induced during the normal female reproductive cycle by estradiol and synthesised in the outer follicular layer of the oocytes. Female rainbow trout injected with E2 had disturbed development of the ovary and had delayed sexual maturity compared to controls. Sustained high circulating levels of vitellogenin before the actual period of natural vitellogenesis, which can be induced by exogenous exposure to estrogens or xenoestrogens, might therefore prevent a normal development of the oocytes. No studies have been published which have concentrated on the effect of sewage effluent exposure on the fertility of female fish.
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